Abraham Lincoln may have suffered from a genetic disorder that literally shattered his nerves, a new study on worms suggests.

Many of the president's descendants have a gene mutation that affects the part of the brain controlling movement and coordination, researchers discovered last year.

The mutation prevents nerve cells from "communicating" with each other properly, but scientists weren't sure exactly how or why.

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The malformed protein could actually be causing nerve cells to break altogether, show the experiments announced today by scientists at the University of Utah.

If Honest Abe had the disease, it would explain the gangly walk for which he was famous, they said.

Humans produce four protein genes called beta spectrin, which help our cells regulate walking and talking and anything else requiring movement.

Normally, wire-like axons that connect each nerve cell flex and bend when we do.

The mutation of one of the beta-spectrin genes causes the degenerative nerve disorder spinocerebellar ataxia type 5 (SCA5), which researchers at the University of Minnesota found in 90 out of 299 of Lincoln's living descendants in a 2006 test.

Those afflicted with ataxia lose coordination and sometimes end up confined to a wheelchair.

Until now, most scientists thought ataxia occurred because nerve cells didn't have beta spectrin linking them together with the same strength they do in a healthy individual.

Nematode worms also produce beta spectrin. When researchers removed the beta spectrin gene from worms, however, the worms' wiry cell axons didn't just malfunction — they severed.

The very same thing could be happening in humans, the University of Utah biologists speculate.

"It's incredible and so very simple that this one protein is what keeps neurons from breaking in your body," said study author Michael Bastiani of the University of Utah's Brain Institute. "The entire functioning of the nervous system depends on these wire-like axons between nerve cells."

The whisper-thin axon is the least complex part of a nerve cell, Bastiani explained, so scientists often have looked elsewhere when searching for the cause of nervous disorders such as ataxia.

Lincoln's trademark lumbering and awkward gait — noted by several historians of his time — would have been a symptom of ataxia, said the University of Minnesota researchers, whose hereditary study pegged his chances of having the disease at about one-in-four.

If he did suffer from ataxia, it was probably in its early stages by the time he was assassinated at age 56 in 1865, said Erik Jorgensen, scientific director of the Brain Institute.

Most nerve cells in the worms studied weren't broken in the embryonic stage, despite the lack of beta spectrin, but began snapping as the worms grew larger. Beta spectrin is only necessary to prevent breakage in mature cells and not to create new ones, the study showed.

Since it is continuous movement over time that causes axons to shatter, without the protective coating of the protein Lincoln's unsteady and irregular way of getting around would probably have gotten much worse had he lived into old age.

The wayward beta spectrin gene could be the culprit in many other neurodegenerative disorders such as Alzheimer's disease, the researchers said, though further testing is needed.

The study's full findings are published in the most recent edition of The Journal of Cell Biology.

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